Alain Lilienbaum

Paris, France

Last Updated: 09/26/2026

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Found 13 publications

Quantification of Exercise-Induced Sarcomeric Damage in R349P Desmin Knock-In Mice: A New Approach in Myofibrillar Myopathy Research.

Quantification of Exercise-Induced Sarcomeric Damage in R349P Desmin Knock-In Mice: A New Approach in Myofibrillar Myopathy Research.

Journal: Neuropathology and applied neurobiology
Published: February 08, 2025

R405W Desmin Knock-In Mice Highlight Alterations of Mitochondria, Protein Quality Control and Myofibrils in Myofibrillar Myopathy.

R405W Desmin Knock-In Mice Highlight Alterations of Mitochondria, Protein Quality Control and Myofibrils in Myofibrillar Myopathy.

Journal: Journal of cachexia, sarcopenia and muscle
Published: October 21, 2024

Desmin Modulates Muscle Cell Adhesion and Migration.

Desmin Modulates Muscle Cell Adhesion and Migration.

Journal: Frontiers in cell and developmental biology
Published: September 26, 2021

Vimentin: Regulation and pathogenesis.

Vimentin: Regulation and pathogenesis.

Journal: Biochimie
Published: August 30, 2021

Absence of Desmin Results in Impaired Adaptive Response to Mechanical Overloading of Skeletal Muscle.

Absence of Desmin Results in Impaired Adaptive Response to Mechanical Overloading of Skeletal Muscle.

Journal: Frontiers in cell and developmental biology
Published: January 31, 2021

Dual Functional States of R406W-Desmin Assembly Complexes Cause Cardiomyopathy With Severe Intercalated Disc Derangement in Humans and in Knock-In Mice.

Dual Functional States of R406W-Desmin Assembly Complexes Cause Cardiomyopathy With Severe Intercalated Disc Derangement in Humans and in Knock-In Mice.

Journal: Circulation
Published: October 07, 2020

Desmin prevents muscle wasting, exaggerated weakness and fragility, and fatigue in dystrophic mdx mouse.

Desmin prevents muscle wasting, exaggerated weakness and fragility, and fatigue in dystrophic mdx mouse.

Journal: The Journal of physiology
Published: November 08, 2019

Alterations of redox dynamics and desmin post-translational modifications in skeletal muscle models of desminopathies.

Alterations of redox dynamics and desmin post-translational modifications in skeletal muscle models of desminopathies.

Journal: Experimental cell research
Published: January 09, 2019

Myofibrillar Myopathies: New Perspectives from Animal Models to Potential Therapeutic Approaches.

Myofibrillar Myopathies: New Perspectives from Animal Models to Potential Therapeutic Approaches.

Journal: Journal of neuromuscular diseases
Published: March 09, 2017

The transcription coactivator ASC-1 is a regulator of skeletal myogenesis, and its deficiency causes a novel form of congenital muscle disease.

The transcription coactivator ASC-1 is a regulator of skeletal myogenesis, and its deficiency causes a novel form of congenital muscle disease.

Journal: Human molecular genetics
Published: December 24, 2015

Antioxidant Treatment and Induction of Autophagy Cooperate to Reduce Desmin Aggregation in a Cellular Model of Desminopathy.

Antioxidant Treatment and Induction of Autophagy Cooperate to Reduce Desmin Aggregation in a Cellular Model of Desminopathy.

Journal: PloS one
Published: March 16, 2015

Advances in the understanding of skeletal muscle weakness in murine models of diseases affecting nerve-evoked muscle activity, motor neurons, synapses and myofibers.

Advances in the understanding of skeletal muscle weakness in murine models of diseases affecting nerve-evoked muscle activity, motor neurons, synapses and myofibers.

Journal: Neuromuscular disorders : NMD
Published: March 06, 2014
Showing 1-12 of 13

Last Updated: 09/26/2026